Detrusor myectomy for detrusor overactivity: a minimum 1-year follow-up



To evaluate the clinical and urodynamic outcome of partial detrusor myectomy in patients with idiopathic detrusor instability and neuropathic hyper-reflexia.

Patients and methods

Seventeen patients with idiopathic detrusor instability and 10 with hyper-reflexia and symptoms not responding to non-surgical treatment underwent partial detrusor myectomy. The clinical and urodynamic results before and after myectomy were compared and the patient’s subjective assessment of the outcome documented.


There was an overall improvement in 17 of 27 patients (63%) but the success rate was higher in those with idiopathic instability (12 of 17) than in those with neuropathy (five of 10). There was urodyn-amic evidence of reduced bladder contractility and an improvement in the storage characteristics of the bladder in most of the patients treated.


Partial detrusor myectomy is relatively simple and is associated with minimum morbidity and an acceptable success rate. The procedure alters the urodynamic behaviour of the bladder and leads to symptomatic and objective improvement, giving better results with idiopathic than with neuropathic detrusor overactivity. Detrusor myectomy may be offered to patients with detrusor overactivity unresponsive to conventional management. The option of enterocysto-plasty is still open to patients with an unsuccessful outcome. However, the long-term results and surgical variations of the technique should be evaluated further.


The bladder overactivity in patients with idiopathic bladder instability and neuropathic detrusor hyper-reflexia may lead to urgency, urge incontinence and frequency, thereby severely impairing the quality of life of some patients. While most patients are managed adequately with anticholinergic therapy and behavioural treatment, a proportion need surgical intervention. Enterocystoplasty is the standard surgical procedure in these patients, but in view of the side-effects of this procedure, e.g. mucus production, bacteri-uria, metabolic changes, bowel disturbances and the potential for neoplastic transformation [1], alternative surgical methods are being explored. Bladder autoaug-mentation by detrusor myectomy was described by Cartwright and Snow [2] as an appropriate alternative in these patients. Most of the reports published to date deal with patients suffering from neuropathic vesicourethral dysfunction [3][4][5][6]. We report our results with partial detrusor myectomy in a series of patients with bladder overactivity secondary to idiopathic or neuropathic aetiology.

Patients and methods

Twenty-seven patients underwent partial detrusor myec-tomy between November 1992 and August 1995; the aetiology of bladder overactivity was idiopathic detrusor instability in 17 and neuropathic hyper-reflexia in 10 (spina bifida in five, spinal cord injury in one, multiple sclerosis in two and transverse myelitis in two). All the patients had been symptomatic for >2 years and were treated initially with conventional methods, i.e. bladder drill or pharmacological treatment, with no benefit. The pre-operative counselling included a discussion of the options available and detrusor myectomy was offered as an alternative to clam cystoplasty. The experimental nature of the procedure was explained to the patients. The possible need for intermittent self-catheterization and the likelihood of further surgery was discussed. Patients were assessed clinically and using standard urodynamic methods. Neuropathic patients were assessed using slow-filling cystometry at filling speeds of 10 mL/min and moderate filling speeds of 50 mL/min were used in patients with idiopathic instability.
Through a Pfannenstiel incision, the bladder was exposed using an extraperitoneal approach. The peritoneum was dissected off the dome of the bladder. After distending the bladder with 250 mL of saline, an area with a diameter of 8-12 cm was marked on the dome of the bladder. A disk of detrusor muscle in this area was excised by careful dissection, leaving the mucosa intact, thereby creating a broad-based mucosal diverticu-lum. There was a distinct network of fine vessels running through the mucosa (Fig. 1) and the detrusor muscle could then be removed in one, two or four different pieces. Any mucosal tears were repaired with 6/0 chromic catgut sutures. Through a small incision in the peritoneum, the greater omentum was drawn out and sutured to the remaining anterior bladder wall. The bladder was drained post-operatively with an indwelling urethral catheter.
Disk of detrusor muscle excised from the bladder

Fig. 1. A disk of detrusor muscle being excised from the dome of the bladder. A fine network of submucosal vessels is visible on the surface of the mucosa.

Cystography was performed 7 days after surgery, before removing the catheter, and patients were assessed at monthly intervals thereafter. Repeat urodynamics were performed at 3-6 months and again at 1 year. The patients were categorized subjectively into three groups as failed, improved or cured, the assessment being prospective and based on the patients’ perception of the symptomatic improvement. Patients were considered cured if they were completely continent, and as improved if there was a reduction in the number of episodes of urgency and/or urge incontinence. The subjective assessment was corroborated where possible by examining voiding diaries. The urodynamic measurements assessed included maximum flow rate, volume at first unstable contraction during filling, maximum amplitude of unstable contraction, cystometric capacity, detrusor pressure at maximum flow and residual urine volume. The mean follow-up for the series was 27 months (range 12-42). Differences between pre- and post-operative urodynamic variables were assessed for statistical significance using Wilcoxon’s signed-ranks test.


Eight patients sustained mucosal perforations intra-operatively which were easily repaired. The subjective outcome at the most recent follow-up was that seven patients were cured and 10 improved; 10 were deemed to have experienced no change in their status. Analysis of the pre- and post-operative voiding diaries of the successful patients showed a reduction in the mean values of day-time frequency (12 and 7, respectively), and episodes of urgency (5 and 2). Subsequent operative procedures performed in patients who failed to respond included enterocystoplasty in three neuropathic patients, who showed no improvement in bladder compliance 12 months post-operatively. Two patients with detrusor instability and interstitial cystitis underwent cystectomy after detrusor myectomy produced no improvement. Two patients required intermittent self-catheterization de novo after myectomy. Two of five patients who had nocturnal enuresis were cured of the condition. Thus, the overall success rate for the group was 63% (17/27) but was greater in those with idiopathic (12 of 17 cured or improved) than in those with neuropathic instability (five of 10 cured or improved).
The urodynamic measurements (Table 1) showed that four patients had a complete resolution of unstable bladder activity, whereas the rest had persistent unstable contractions of various degrees. Overall, there were significant changes in all the urodynamic measurements, but the difference between the idiopathic and neuropathic groups was not statistically significant.
Table 1 The results of the urodynamic assessment before and after myectomy

Before (Mean [SD]) After (mean [SD]) P
Volume at first unstable wave (mL) 108 (56) 177 (114) <0.01
Max. amplitude of unstable wave (cmH O) 65 (47) 30 (23) 0.004
Cystometric capacity (mL) 209 (129) 271 (149) < 0.01
Detrusor pressure at max. flow (cmH O) 83 (56) 52 (25) < 0.001
Residual urine (mL) 13 (20) 64 (53) < 0.001


Since its initial description, detrusor myectomy has been performed by various authors with variable results, the reported success rates being up to 80% [3][4][5][6]. Stothers et al. [7] showed that detrusor myotomy yielded results equal to those from detrusor myectomy in experimental and clinical situations. The objective improvements documented previously include abolition or reduction in unstable bladder activity, increased cystometric capacity, increased bladder compliance, reduction of voiding pressures and improvement of VUR. The present results confirm those reported previously, including a significant reduction in the mean values of volume at first unstable contraction, maximum amplitude of unstable contraction, and significant increase in the mean cystometric capacity. The significant reduction in the voiding pressures and increase in residual volume also agree with previous observations.
The urodynamic results can be compared with those after clam enterocystoplasty. Kockelbergh et al. [8] found no significant change in the urodynamic measurements of bladder capacity, residual volume, voiding pressure and flow rates in a series of 45 patients predominantly with idiopathic instability treated with enterocystoplasty. However, Hasan et al. [9] found significant improvements in cystometric capacity, from 242 to 330 mL, in a mixed series of patients with idiopathic (13) and neuropathic (35) bladder dysfunction. Clam enterocystoplasty has also been shown to produce a significant reduction in voiding pressures [10].
The subjective improvement obtained with detrusor myectomy is inferior to that documented for clam enter-ocystoplasty, which had been shown to produce an early symptomatic improvement in 98% of patients treated for idiopathic or neuropathic bladder dysfunction [9]. Although the clinical outcome is not as good as that with enterocystoplasty, those patients who respond to detrusor myectomy would have been spared the side-effects of intestinal interposition into the urinary tract, which include mucus production, infection and the potential for neoplastic change in the long-term. Those who do not respond still have the option of enterocystoplasty.
Filling and voiding cystogram after detrusor myectomy
Fig. 2. Filling and voiding cystogram after detrusor myectomy; the broad-based mucosal diverticulum, outlined by arrows, may act as a buffering mechanism against detrusor overactivity.
The mechanism by which detrusor myectomy operates is speculative. The various urodynamic changes documented suggest that the procedure may owe its beneficial effect to reduced detrusor contractility and the “pop-off” mechanism of the newly created mucosal diverticulum (Fig. 2). To avoid the perivesical fat and peritoneum preventing distension of the mucosal diverticulum, and to facilitate any later surgery, we performed omentopla-sty whenever the greater omentum was available. In patients requiring re-operation after myectomy, the greater omentum protects against perivesical fibrosis. In one patient in whom omentum was not used because it was not available, the bladder mucosa became firmly adhered to the retropubic area, thereby losing the distensibility of the diverticulum. The value of postoperative bladder cycling is not known. Recently, we have practised regular distension with normal saline in patients without intra-operative mucosal disruption.
The eventual fate of the mucosal diverticulum is also speculative; the present results suggest that there is progressive distension, with an incremental improvement in clinical and urodynamic observations in some patients in this series. However, it is possible that regrowth of detrusor muscle or perivesical fibrosis may lead to long-term failure. In animal experiments, the regenerative capacity of bladder muscle has been documented [11] and may imply that the detrusor muscle could cover the mucosal diverticulum by organized regrowth of muscle. Sequential CT may be useful in documenting the fate of the muscular defect, especially when omentoplasty has been performed.
In the present patients, the clinical outcome was worse in those with neuropathic than with idiopathic instability. The reported results of myectomy in neuropathic patients are contradictory; Kaufman et al. [12] concluded that detrusor myectomy failed in all 11 myelodysplastic patients in their series, after a mean follow-up of 16 months. This contrasts with the excellent improvement reported by Stohrer et al. [4] in a series of neuropathic patients, and the good results reported by Milam et al. [13] in a mixed series of 13 patients with idiopathic and neuropathic dysfunction. The latter authors reported that seven of 13 patients became dry, four improved and two were unchanged after a mean follow-up of 13.6 months. Interestingly, all three patients who required enterocystoplasty in the present series were neuropaths; the reasons for the higher failure rate noted in neuropaths is unknown. The relatively low efficacy may be related to the inability of neuropathic patients to perform bladder training because they have reduced/absent bladder sensation, allowing gradual enlargement of the diverticulum.
Although there were few complications after the intermediate follow-up, potential problems associated with this operation are worth considering. The increasing residual volumes may predispose to recurrent urinary tract infections and may necessitate intermittent self-catheterization. There may be an increased risk of spontaneous and catheter-induced perforation in these patients, and precautions need to be taken to avoid such problems.
In summary, detrusor myectomy is simple to perform and seems to give satisfactory results in patients with idiopathic detrusor instability in the medium term. It seems an ideal alternative to enterocystoplasty in this group, especially because many urologists are reluctant to perform the latter for idiopathic instability, and leaves the option of enterocystoplasty in patients not responding to myectomy. In the neuropathic group, the results are less encouraging. The long-term results of myectomy should be evaluated rigorously before its role is defined.


The authors thank Miss Ruth Thomas, Research Assistant, Health Services Research Unit, University of Aberdeen, for her help in the statistical analysis.


  • K.S. Swami, MS, MCh, FRCSEd (Urol), formerly Clinical Research Fellow, now Consultant Urologist.
  • R.C.L. Feneley, MA, MChir, FRCS, Consultant Urologist.
  • J.C. Hammonds, FRCS, Consultant Urologist.
  • P. Abrams, MD, FRCS, Consultant Urologist.
  • Correspondence: Mr K.S. Swami, Aberdeen Royal Infirmary, Forresterhill, Aberdeen AB25 2ZB, UK.


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